Murali Chakinala, MD, FCCP

Panelists discuss how sotatercept represents a paradigm shift as the first activin signaling inhibitor showing dramatic improvements in heavily pretreated patients, with the Stellar and Zenith trials demonstrating significant reductions in clinical worsening and potential for reverse remodeling.

Panelists discuss how riociguat targets the nitric oxide pathway and is approved for both Group 1 PAH and Group 4 chronic thromboembolic pulmonary hypertension, with specific patient selection criteria based on risk stratification and surgical candidacy.

Panelists discuss how current therapeutic strengths include 15 approved treatments with different mechanisms of action that can work synergistically, while limitations involve variable delivery methods and complexity, leading to more aggressive upfront combination therapy approaches.

Panelists discuss how treatment individualization depends on patient-specific factors including age, comorbidities, disease severity, and personal preferences, balancing clinical guidelines with shared decision-making to optimize both efficacy and adherence.

Panelists discuss how disease progression monitoring requires integrating multiple data points including symptoms, six-minute walk tests, biomarkers like BNP/NT-proBNP, and imaging studies, with risk stratification tools helping guide treatment decisions while considering individual patient characteristics.

Panelists discuss how early detection barriers include nonspecific symptoms like progressive dyspnea that are often misattributed to more common conditions, leading to delayed diagnosis and the need for improved diagnostic algorithms using biomarkers and imaging.

Panelists discuss how pulmonary arterial hypertension diagnosis requires comprehensive evaluation including right heart catheterization to confirm hemodynamic criteria, with normal mean PA pressure being ≤20 mmHg and the need to rule out other causes of pulmonary hypertension.

Panelists discuss how the pathophysiology of pulmonary arterial hypertension involves complex mechanisms across multiple genetic and treatment pathways, with over 20 identified genes and four major therapeutic targets including nitric oxide, endothelin, prostacyclin, and activin signaling inhibition.